Science advances · 2026
Intestinal fructose catabolism promotes obesity and insulin resistance via ileal lacteal remodeling.
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Lopez Miranda L, Kang Taekyung, Espeleta Ana M, Rubtsova Varvara I, Baek Jongwon, Songcuan Jakob, Moyer Elena M, Kim Joohwan, Song Won-Suk, Jung Sunhee, Lai Rochelle W, Binuya Aiyana, Lee Christopher H, Lantz Amy R, D'Sa Nicholas, Anica Alexis, Tran Elise, Chun Yujin, Choi Wonsuk, Jang Ki-Hong, Cho Sungji, Kelly Miranda E, Tamburini Ian J, Alam Yasmine H, Le Johnny, Ramirez Cuauhtemoc B, Kataru Raghu P, Hong Seon Pyo, de Aguiar Vallim Thomas Q, Nicholas Dequina A, Xue Katherine S, Lee Gina, Bae Hosung, Jang Cholsoon
Аннотация
High-fructose corn syrup (HFCS) consumption is a risk factor for obesity and diabetes, yet the underlying mechanisms, especially at the specific organ level, are incompletely understood. Catabolism of dietary fructose primarily occurs in the small intestine and liver, with fructose breakdown in the liver being pathological, while small intestinal fructose clearance protects the liver. Here, we report that inhibition of fructose catabolism specifically in the murine small intestine unexpectedly mitigates fructose-induced obesity and insulin resistance. Such phenotypes are attributed to decreased dietary fat absorption by the shortening of ileal lacteals. Fecal transplantation experiments revealed that the microbiome altered by blunted host intestinal fructose catabolism decreases ileal macrophages essential for lacteal growth. Thus, altered intestinal lacteal architecture likely contributes to the synergistic effects of high fat and sugar on metabolic disorders. It may also be relevant to the clinical evidence that pharmacologic suppression of fructose catabolism mitigates diet-induced obesity.